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KCNK3 encodes a member of the superfamily of potassium channel proteins that contain two pore-forming P domains. Additionally we are shipping Potassium Channel, Subfamily K, Member 3 Antibodies (127) and many more products for this protein.
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The results of the present study suggested that miR138 promoted proliferation and suppressed mitochondrial depolarization of human pulmonary artery smooth muscle cells by targeting TASK1.
Screening for mutations in the human TASK-1 gene in 155 cases of sudden infant death syndrome (SIDS) was inconclusive. Results are suggestive for an increased hypoxia-sensitivity of neonatal TASK-1(-/-) mice, however, without causing an increase in neonatal lethality. In adult female TASK-1(-/-) mice respiration was unaffected, whereas adult male TASK-1(-/-) mice showed a modified breathing pattern.
Recent studies show that modulation of TASK-1 channels, either directly or indirectly by targeting their regulatory mechanisms, has the potential to control pulmonary arterial tone in humans. Furthermore, mutations in KCNK3 have been identified as a rare cause of both familial and idiopathic pulmonary arterial hypertension. [review]
Sequencing of BMPR2 (show BMPR2 Proteins), CAV1 (show CAV1 Proteins), and KCNK3 coding regions did not identify any pathogenic variants in these genes in infants with pulmonary hypoplasia and pulmonary hypertension.
Heterozygous KCNK3 mutations in pulmonary arterial hypertension lead to variable loss of channel function via distinct mechanisms.
Familial cases of Pulmonary Arterial Hypertension related to heterozygous missense variants in the KCNK3 gene (encoding the two-pore-domain potassium channel (show KCNAB2 Proteins) TASK-1) has been described with a prevalence of 1.3 and 3.2% in idiopathic Pulmonary Arterial Hypertension and heritable Pulmonary Arterial Hypertension, respectively.
our study indicates that TASK-1 is functionally regulated by caveolin-3 (show CAV3 Proteins), possibly via association with each other on the cell surface. These results point out a novel mechanism in the regulation of TASK-1.
A burden of rare variants in BMPR2 (show BMPR2 Proteins) significantly contributed to the risk of pulmonary arterial hypertension. In the remaining one family, the patient carried a pathogenic variant in a member of potassium channels, KCNK3, which was the first replicative finding of channelopathy in an Asian population.
The results suggested that heterodimerization of TASK1 and TALK2 provides cells with the ability to make multiple responses to a variety of physiological and pharmacological stimuli.
Genetic variation in the KCNK3 gene may contribute to Blood pressure variation and less severe Hypertensive disorders in which aldosterone may be one of several causative factors
Whereas adult female TASK-1-/- mice had a virtually normal respiratory phenotype, except for an increased relaxation time, adult male TASK-1-/- mice exhibited enhanced ventilation that was mainly due to an increased tidal volume. Respiratory responses to hypercapnia and hypoxia were largely preserved. In neonatal TASK-1-/- mice, respiratory drive appeared reduced and knockout animals were more prone to experience apnea.
Acute hypercapnia (5% CO2) stimulated ventilation in TASK-1/3(-/-) and wild-type mice to a similar extent; however, at higher CO2 concentrations the stimulation of ventilation was more pronounced in TASK-1/3(-/-) mice. At hyperoxia (100% O2), TASK-1(-/-), TASK-3 (show KCNK9 Proteins)(-/-) and wild-type mice showed the physiological small decrease of ventilation. TASK-1/3(-/-) mice exhibited an abnormal increase of ventilation under hyperoxia.
Our results have uncovered a previously unknown role of c-Src tyrosine kinase (show CSK Proteins) in regulating interneuron function in the brain and identified a novel mechanism by which TASK-1 channels are activated in neurons.
Adipose-specific Kcnk3 knockout mice display increased energy expenditure and are resistant to hypothermia and obesity.
While there is compelling evidence that TASK-1 is involved in the pathogenesis of pulmonary arterial hypertension in humans, the mouse does not appear to serve as a suitable model to study the underlying molecular mechanisms
the K(+) channel (show KCNC4 Proteins) TASK1 controls the thermogenic activity in brown adipocytes through modulation of beta-adrenergic receptor signaling.
KCNK3 channels are not involved in hearing.
An important role for TASK-1 channels in limiting pancreatic alpha-cell excitability and glucagon (show GCG Proteins) secretion during glucose stimulation.
A glucose-dependent role for beta-cell TASK-1 channels of limiting glucose-stimulated Deltapsip depolarization and insulin (show INS Proteins) secretion, which modulates glucose homeostasis.
Oxygen and mitochondrial inhibitors modulate both monomeric and heteromeric TASK-1 and TASK-3 (show KCNK9 Proteins) channels in mouse carotid body type-1 cells.
This gene encodes a member of the superfamily of potassium channel proteins that contain two pore-forming P domains. The encoded protein is an outwardly rectifying channel that is sensitive to changes in extracellular pH and is inhibited by extracellular acidification. Also referred to as an acid-sensitive potassium channel, it is activated by the anesthetics halothane and isoflurane. Although three transcripts are detected in northern blots, there is currently no sequence available to confirm transcript variants for this gene.
potassium channel subfamily K member 3
, TWIK-related acid-sensitive K(+) channel 1
, TWIK-related acid-sensitive K+ channel
, acid-sensitive potassium channel protein TASK
, acid-sensitive potassium channel protein TASK-1
, cardiac potassium channel
, potassium inwardly-rectifying channel, subfamily K, member 3
, two P domain potassium channel
, two pore K(+) channel KT3.1
, two pore potassium channel KT3.1
, cardiac two pore background K(+) channel
, TASK-1 potassium channel